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Background: Deep brain stimulation (DBS) of the nucleus basalis of Meynert (NBM) has shown potential for the treatment of mild-to-moderate Alzheimer's disease (AD). However, there is little evidence of whether NBM-DBS can improve cognitive functioning in patients with advanced AD. In addition, the mechanisms underlying the modulation of brain networks remain unclear. This study was aimed to assess the cognitive function and the resting-state connectivity following NBM-DBS in patients with advanced AD. Methods: Eight patients with advanced AD underwent bilateral NBM-DBS and were followed up for 12 months. Clinical outcomes were assessed by neuropsychological examinations using the Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale. Resting-state functional magnetic resonance imaging and positron emission tomography data were also collected. Results: The cognitive functioning of AD patients did not change from baseline to the 12-month follow-up. Interestingly, the MMSE score indicated clinical efficacy at 1 month of follow-up. At this time point, the connectivity between the hippocampal network and frontoparietal network tended to increase in the DBS-on state compared to the DBS-off state. Additionally, the increased functional connectivity between the parahippocampal gyrus (PHG) and the parietal cortex was associated with cognitive improvement. Further dynamic functional network analysis showed that NBM-DBS increased the proportion of the PHG-related connections, which was related to improved cognitive performance. Conclusion: The results indicated that NBM-DBS improves short-term cognitive performance in patients with advanced AD, which may be related to the modulation of multi-network connectivity patterns, and the hippocampus plays an important role within these networks. Trial registration: ChiCTR, ChiCTR1900022324. Registered 5 April 2019—Prospective registration. https://www.chictr.org.cn/showproj.aspx?proj=37712 [ABSTRACT FROM AUTHOR]

• TWNK mutation patients presenting with generalized dystonia who underwent deep brain stimulation are reported. • Local field potential is more closely related to the clinical syndrome than specific disease. • Deep brain stimulation can inhibit the TWNK mutation patients' pathological oscillations. We focused on a rare gene mutation causing dystonia in two siblings who received globus pallidus internus deep brain stimulation (GPi-DBS). The aim was to characterize the relationship between neuronal activity patterns and clinical syndromes. Whole exome sequencing was applied to identify the TWNK (previous symbol C10orf2) mutation; Two siblings with TWNK mutation presented as generalized dystonia with rigidity and bradykinesia; four other sporadic generalized dystonia patients underwent GPi-DBS and local field potentials (LFPs) were recorded. Oscillatory activities were illustrated with power spectra and temporal dynamics measured by the Lempel-Ziv complexity (LZC). Normalized power spectra of GPi LFPs differed between patients with TWNK mutation and dystonia over the low beta bands. Patients with TWNK mutation had higher low beta power (15–27 Hz, unpaired t-test, corrected P < 0.0022) and lower LZC (15–27 Hz, unpaired t-test, P < 0.01) than other patients with generalized dystonia. On the other hand, the TWNK mutation patients showed decreased low frequency and beta oscillation in the GPi after DBS, as well as improved movement performance. The LFPs were different in TWNK mutation dystonia siblings than other patients with generalized dystonia, which indicate the abnormal LFPs were related to symptoms rather than specific disease. In addition, the inhibited effect on oscillations also provided a potential evidence for DBS treatment on rare movement disorders. This study could potentially aid in the future development of adaptive DBS via rare disease LFPs comparison. [ABSTRACT FROM AUTHOR]

Background The efficacy of anterior thalamic nuclei (ANT) deep brain stimulation (DBS) in mitigating epileptic seizures has been established. Though the neuroprotection of ANT-DBS has been illustrated, the seizure mitigating mechanism of ANT-DBS has not been thoroughly elucidated. In particular, the effect of ANT-DBS on neurogenesis has not been reported previously. Method Thirty-two male Sprague Dawley rats were randomly assigned to the following groups: sham-DBS-healthy (HL) (n = 8), DBS-HL (n = 8), sham-DBS-epilepsy (EP) (n = 8) and DBS-EP (n = 8). Normal saline and kainic acid were injected, respectively, into the former and later two groups, and seizures were monitored. One month later, rats received electrode implantation. Stimulation was exerted in the DBS group but not in the sham-DBS group. Next, all rats were sacrificed, and the ipsilateral hippocampus was dissected and prepared for quantitative real time PCR (qPCR) and western blot analysis in order to measure neuronal nuclear (NeuN), brain-derived neurotrophic factor (BDNF), doublecortin (DCX) and Ki-67 expressions. Results A 44.4% seizure frequency reduction was obtained after ANT-DBS, and no seizures was observed in healthy rats. NeuN, BDNF, Ki-67 and DCX expression levels were significantly decreased in the epileptic rats compared to healthy rats ( P < 0.01 or P < 0.05). Obvious increases in NeuN, Ki-67 and DCX expressions were observed in epileptic and healthy rats receiving stimulation compared to rats receiving no stimulation (all Ps < 0.01). However, BDNF expression was not affected by ANT-DBS (all Ps > 0.05). Conclusions (1) ANT-DBS reduces neuronal loss during the chronic stage of epilepsy. (2) Neurogenesis is elevated by ANT-DBS in both epileptic and healthy rats, and this elevation may not be regulated via a BDNF pathway. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies found subthalamic nucleus deep brain stimulation (STN‐DBS) has clinical effect on Parkinson's disease, dystonia, and obsessive compulsive disorder. It is noteworthy that only a few studies report the STN‐DBS for Tourette's syndrome (TS). Globus pallidus interna (GPi)‐DBS is the one of the most common targets for TS. So, this paper aims to investigate the neural oscillations in STN and GPi as well as the DBS effect between these two targets in same patients. Methods: The local field potentials (LFPs) were simultaneously recorded from the bilateral GPi and STN in four patients with TS. The LFPs were decomposed into neural oscillations, and the frequency and time–frequency characteristics of the neural oscillations were analyzed across the conditions of resting, poststimulation, and movement. Results: No difference of resting LFP was found between the two targets. The poststimulation period spectral power revealed the high beta and gamma oscillations were recovered after GPi‐DBS but remained attenuated after STN‐DBS. The STN beta oscillation has fewer changes during tics than voluntary movement, and the gamma oscillation was elevated when the tics appeared. Conclusion: The high beta and gamma oscillations in GPi restored after GPi‐DBS, but not STN‐DBS. High beta and gamma oscillations may have physiological function in resisting tics in TS. The cortex compensation effect might be interfered by the STN‐DBS due to the influence on the hyper‐direct pathway but not GPi‐DBS. [ABSTRACT FROM AUTHOR]